Literature summary for 2.1.1.354 extracted from

Ortega-Molina, A.; Boss, I.W.; Canela, A.; Pan, H.; Jiang, Y.; Zhao, C.; Jiang, M.; Hu, D.; Agirre, X.; Niesvizky, I.; Lee, J.E.; Chen, H.T.; Ennishi, D.; Scott, D.W.; Mottok, A.; Hother, C.; Liu, S.; Cao, X.J.; Tam, W.; Shaknovich, R.; Garcia, B.A.; Gascoyne, R.D.; Ge, K.; Shilatifard, A.; Elemento, O.; Nussenzweig, A.; Melnick, A.M.; Wendel, H.G.
The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development (2015), Nat. Med., 21, 1199-1208.

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q6PDK2	-	-

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
S-adenosyl-L-methionine + histone H3(K4)	-	Mus musculus	S-adenosyl-L-homocysteine + N-methylated histone H3(K4)	-	?

Synonyms	Comment	Organism
KMT2D	-	Mus musculus

General Information	Comment	Organism
physiological function	isoform KMT2D functions as a bona fide tumor suppressor and its genetic ablation in B cells promotes lymphoma development in mice. KMT2D deficiency also delays germinal center involution and impedes B cell differentiation and class switch recombination. KMT2D affects methylation of lysine 4 on histone H3 (H3K4) and expression of a set of genes, including those in the CD40, JAK-STAT, Toll-like receptor and B cell receptor signaling pathways. Other KMT2D target genes include frequently mutated tumor suppressor genes such as TNFAIP3, SOCS3 and TNFRSF14	Mus musculus

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Release 2023.1 (January 2023)